Project description:The bZIP transcription factor ATF6α is a master regulator of endoplasmic reticulum (ER) stress response genes. In this report, we identify the multifunctional RNA polymerase II transcription factor Elongin as a cofactor for ATF6α-dependent transcription activation. Biochemical studies reveal that Elongin functions at least in part by facilitating ATF6α-dependent loading of Mediator at the promoters and enhancers of ER stress response genes. Depletion of Elongin from cells leads to impaired transcription of ER stress response genes and to defects in the recruitment of Mediator and, in particular, its CDK8 kinase subunit. Taken together, these findings bring to light a new role for Elongin as a loading factor for Mediator during the ER stress response.
Project description:The bZIP transcription factor ATF6α is a master regulator of endoplasmic reticulum (ER) stress response genes. In this report, we identify the multifunctional RNA polymerase II transcription factor Elongin as a cofactor for ATF6α-dependent transcription activation. Biochemical studies reveal that Elongin functions at least in part by facilitating ATF6α-dependent loading of Mediator at the promoters and enhancers of ER stress response genes. Depletion of Elongin from cells leads to impaired transcription of ER stress response genes and to defects in the recruitment of Mediator and, in particular, its CDK8 kinase subunit. Taken together, these findings bring to light a new role for Elongin as a loading factor for Mediator during the ER stress response.
Project description:In order to determine that CUT&Tag is similar to known DUX ChIP-seq, we performed CUT&Tag with a mCherry-tagged DUX (with the mCherry antibody). Once confirmed, we pewrformed CUT&Tag for other DUX derivatives with their mCherry tag Then, we performed CUT&Tag for H3K9ac, which is known to globally increase in 2-cell-like cells, which occurs after DUX expression, and CUT&Tag for SMARCC1, a subunit of the SWI/SNF complex
Project description:To investigate the enrichment of SMARCA4-R1157W mutation on downstream target gene promoters, we performed CUT&Tag experiments in HCT116 cells.